Cardiac energetics, measured by the PCr/ATP ratio, were similarly impaired in hypertrophic cardiomyopathy (1.63) and hypertensive heart disease (1.69) compared to healthy controls (1.97; p<0.001).
Cross-Sectional (n=124)
No
Does cardiac energetic impairment differ between patients with hypertrophic cardiomyopathy and hypertensive heart disease?
HCM and HHD share a similar degree of cardiac energetic impairment, suggesting perturbed myocardial metabolism may drive phenotype development in response to hypertension.
Absolute Event Rate: 1.63% vs 1.97%
p-value: p=<0.001
Abstract Background Distinguishing between hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD) is often challenging due to significant phenotypic overlap. Hypertension may also accelerate phenotypic development in individuals genetically susceptible to HCM, suggesting a direct link between both conditions 1. While energy deficiency and mitochondrial dysfunction are hallmarks of HCM 2, little is known about the impact of hypertension on myocardial energy metabolism. Purpose To compare cardiac energetics between HCM and HHD using cardiovascular magnetic resonance. Methods 124 participants (20 healthy volunteers, 73 patients with non-obstructive HCM, and 31 HHD patients) were recruited as part of a prospective, cross-sectional single-centre study. Multiparametric cardiovascular magnetic resonance was performed at 3T to assess cardiac function and myocardial fibrosis. The cardiac phosphocreatine-to-adenosine triphosphate (PCr/ATP) ratio, a marker of overall cardiac energetics, was measured by ³¹P magnetic resonance spectroscopy. Results 18% of patients with HCM and 16% with HHD were female; both groups had similar age (53±11 vs. 51±14 years, p=0.49) and BMI (29.6±4.8 vs. 31.2±3.5 kg/m², p=0.09). Despite on treatment with a median of 3 1-7 different antihypertensive medications, systolic blood pressure in the HHD cohort remained elevated at 156±22 mmHg. Patients with HCM and HHD had both higher BMI and a higher prevalence of diabetes mellitus compared to controls (6.5 and 5.5 vs. 0%). Maximal wall thickness was significantly greater in HCM than in HHD (19±4 vs. 14±2 mm, p0.001), whereas left ventricular mass was similarly increased (153±48 vs. 157±52g, p=0.76). Compared to controls, the cardiac PCr/ATP ratio was reduced in HCM and HHD, however, no significant differences were observed between both disease groups (1.97±0.32 vs. 1.63±0.37 and 1.69±0.37, p0.001; Figure). Univariate regression analyses indicated no association between impaired cardiac energetics and maximal wall thickness, left ventricular mass index, or systolic function in either HCM or HHD (p for all 0.05). Conclusions HCM and HHD share a similar degree of cardiac energetic impairment, which is not explained by the severity of cardiac hypertrophy. Our findings suggest perturbations of myocardial metabolism as a potential driver of HCM phenotype development in response to arterial hypertension in genetically predisposed individuals, indicating a role as a future target for therapeutic interventions.Summary of key study findings.
Beyhoff et al. (Sat,) conducted a cross-sectional in Hypertrophic cardiomyopathy and hypertensive heart disease (n=124). Cardiovascular magnetic resonance and ³¹P magnetic resonance spectroscopy vs. Healthy volunteers was evaluated on Cardiac phosphocreatine-to-adenosine triphosphate (PCr/ATP) ratio (p=<0.001). Cardiac energetics, measured by the PCr/ATP ratio, were similarly impaired in hypertrophic cardiomyopathy (1.63) and hypertensive heart disease (1.69) compared to healthy controls (1.97; p<0.001).